Vitamin strategy may curb risk of second stroke
NEW YORK (Reuters Health) – A high-dose vitamin supplement
may help reduce the risk of a second stroke, as well as death
and cardiac events, according to a study published in the
journal Stroke this month. The supplement consisted of vitamins
B9 (folate), B6, and B12, which are known to reduce blood
levels of homocysteine — an amino acid linked to heart
In a previous report from the Vitamin Intervention for
Stroke Prevention (VISP) study group, the combined vitamin
therapy did not reduce recurrent stroke and cardiac events, but
it turned out that the trial included patients who were not
likely to benefit from the treatment.
“The VISP trial included patients with deficiency of
vitamin B12 who were unlikely to respond to our treatment, as
well as patients with renal failure, who would not respond as
well to vitamin therapy,” Dr. David J. Spence of the Stroke
Prevention and Atherosclerosis Research Center in Ontario,
Canada told Reuters Health.
When Spence and colleagues re-analyzed the results in a
subgroup of 2,155 subjects deemed most likely to respond to
treatment, the combined vitamin therapy did appear to have a
beneficial effect on recurrence of stroke and cardiac events.
Specifically, the team compared results of low-dose vitamin
versus high-dose vitamin therapy and found that high-dose
vitamin supplements reduced recurrent stroke, death and heart
disease by 21 percent. When they subdivided patients by
baseline levels of vitamin B12, thus identifying those with
difficulties absorbing the vitamin, the differences between the
low-dose and high-dose groups became greater.
“It is too early to conclude that vitamin therapy to lower
total homocysteine is ineffective in the prevention of
cardiovascular events,” said Spence.
He and colleagues suggest that in the modern age in which
grains are fortified with folate, the response to vitamin
therapy for lowering homocysteine largely depends on B12 levels
of the patients. Higher doses of B12, in addition to other
therapies, will be required to reduce homocysteine, and thus to
reduce stroke and the combined end point of stroke, death, and
SOURCE: Stroke, November 2005.